(by B. Roberts)
As with androgens, where any hormone that has the activity of testosterone is an
androgen and therefore all anabolic steroids are androgens, any hormone that has
the activity of estradiol, the principal female sex hormone, is an estrogen. The
most active natural estrogens in humans are estradiol and estrone.
These hormones are related to each other rather similarly to how the andro
prohormones are related to each other. Just as androdiol has a hydroxy (or ???ol)
group at both the 3- and 17- positions, estradiol likewise has a hydroxy group
at those positions. Estrone, like androstenedione, has keto (or ???one, pronounced
"oan") groups at those positions.
Estradiol is the most potent (effective per milligram) of the natural estrogens.
It is produced either from testosterone via the aromatase enzyme, or from
estrone via the estrogenic 17b-HSD enzyme.
Estrone is less potent, but all this means is that one needs more of it to
accomplish the same job. It is produced either from androstenedione via
aromatase, or from estradiol via the same 17b-HSD enzyme working in reverse.
From the standpoint of the bodybuilder using anabolic/androgenic steroids (AAS),
if nothing is done about the situation, high estrogen levels can cause
gynecomastia, will inhibit natural testosterone production, and will cause
bloating. High estrogen levels also make it more difficult to lose fat, and tend
to cause female pattern fat distribution even in males.
Estradiol also has carcinogenic metabolites, and a liver problem sometimes
associated with AAS use, hepatic cholestasis, is caused not by androgen but by
an estrogen metabolite.
It is also not unusual for bodybuilders to feel poorly on beginning a cycle of
high dose testosterone without antiestrogens, and for this reason many have
advocated starting with a low dose and building up. However, I strongly suspect
that the real problem is estrogenic effect on mood, and the problem can be
avoided with use of an aromatase inhibitor.
Though most bodybuilders feel they know which steroids aromatize and which do
not, sometimes the beliefs are in error. This is because progestogenic activity
(activity like that of progesterone, another female hormone) is easily mistaken
for estrogenic activity. Both hormones can cause bloating, and both can cause
gyno. So AAS which are capable of activating not only the androgen receptor but
also the progesterone receptor are often mistakenly assumed to aromatize. (Note:
these androgens do not "convert to progesterone" but rather are themselves,
without any change needed, able to act on that receptor.)
Nandrolone is proven to be a progestin. This fact is of clear importance in
bodybuilding, because while moderate Deca-only use actually lowers estrogen
levels as a consequence of reducing natural testosterone levels and thus
allowing the aromatase enzyme less substrate to work with, Deca nonetheless can
cause gyno in some individuals. Furthermore, just as progesterone will to a
point increase sex drive in women, and then often decrease it as levels get too
high, high levels of progestogenic steroids can kill sex drive in male
bodybuilders, though there is a great deal of individual variability as to what
is too much.
Incidentally, this progestogenic activity also inhibits LH production, and
contrary to common belief, even small amounts of Deca are quite inhibitory,
approximately as much so as the same amount of testosterone.
What relevance does this have to an article on antiestrogens? Well,
antiestrogens can do nothing about these side effects of Deca.
The same appears to be true of oxymetholone (Anadrol) and of norethandrolone
Methenolone (Primobolan), stanozolol (Winstrol), dromostanolone (Masteron),
oxandrolone (Anavar), mesterolone (Proviron), stenbolone (Anatrofin),
trenbolone, and DHT do not aromatize, and thus, antiestrogens are not relevant
to these AAS either.
The steroids where aromatization is of particular concern are testosterone,
methandrostenolone (Dianabol), boldenone (Equipoise), and to some extent
fluoxymesterone (Halotestin). However the latter is usually used in doses low
enough that aromatization is not an issue.
Among the prohormones, androstenedione is the principal offender with regard to
aromatization, being readily converted to estrone. With androdiol, only that
small portion which converts to testosterone can be converted further to
estradiol, and that will occur only in the same percentage that other
testosterone converts to estradiol.
Norandrodiol cannot convert directly to estrogen, and even after conversion to
nandrolone is not readily converted to estrogen.
Norandrostenedione can be converted to estrone by aromatase, but is a very poor
substrate for that enzyme. It can actually act as a competitive inhibitor,
blocking better substrates such as androstenedione or testosterone. It is
possible then, though unproven, that norandrostenedione might have some value as
an aromatase inhibitor in bodybuilding. I do think, however, that the
pharmaceuticals designed for the purpose should be assumed to be better choices.
The most commonly used aromatase inhibitor in bodybuilding is aminoglutethimide
(Cytadren). This drug also inhibits an enzyme (desmolase) necessary for
synthesis of cortisol, but fortunately, aromatase can be inhibited with levels
of drug that cause only limited inhibition of desmolase.
Contrary to popular belief, it is generally not desirable to inhibit cortisol
production. Doing so will likely lead to joint problems, and furthermore once
the inhibition ends, the price of above-normal cortisol production must usually
For an average male, a dose of 250 mg/day (one tablet) appears optimal. The
half-life is 8 hours, so the drug is better taken in divided doses. The best
plan seems to be to take half a tablet on arising, and quarter tabs six and
twelve hours later. This keeps levels generally fairly constant, but allows a
small drop in the hours shortly before arising, which is then compensated for by
the higher dose on arising. With this scheme, inhibition of cortisol production
is generally too low to be noticed, and generally there is no rebound effect on
discontinuance. However it is not a bad idea nonetheless to taper off, first
omitting the midday quarter tab dose for a few days, then omitting both quarter
tab doses, then reducing the initial dose to one quarter tab, and then ending
completely. A week is sufficient for the taper.
Some people suffer a degree of lethargy or sedation from aminoglutethimide, even
at this low dose, but most do not.
Anastrozole (Arimidex) is a superior aromatase inhibitor which does not have the
above side effects. It is, however, very expensive. With moderate doses of
testosterone it seems that 1 mg/day is sufficient, and some have claimed half a
tab to be sufficient. I do not have blood test data to verify that, however.
Clomiphene (Clomid) and tamoxifen (Nolvadex) are the most popular drugs of this
class. They are more precisely referred to as "selective estrogen receptor
modulators." This is because their mode of action is not so simple as merely
blocking the estrogen receptor. Estrogen receptors require not only hormone but
also activation of regions of the receptor called AF-1 and AF-2. AF-1, to be
activated, requires phosphorylation, while AF-2 can be activated by any of a
number of cofactors, such as IGF-1.
As it happens, clomiphene and tamoxifen are estrogen receptor antagonists
(blockers) in cells that depend on activation of the AF-2 region, while in cells
which activate AF-1, these compounds are estrogens.
In some cells these drugs activate one of the types of estrogen receptor (ERa )
but are antagonists of the other type (ERb ).
The result is that these compounds are antiestrogenic in breast tissue, fat
tissue, and in the hypothalamus, which is what we want in bodybuilding, but are
estrogenic in bone tissue and with respect to favorable effect on blood lipid
profile, both of which are, again, desirable. They also appear to have some
estrogenic effect on mood, though this may be in only parts of the brain (the
matter is not studied.)
Cyclofenil is a similar drug to the above two. Clomiphene will do everything
that the other two will do, but for some unknown reason, has been found more
effective than tamoxifen both medically and in bodybuilding for increasing LH
Raloxifene (Evista) is a new selective estrogen receptor modulator that, for
women, has the advantage of being an antiestrogen in the uterus, whereas
clomiphene and tamoxifen are estrogens in that tissue. For this reason, the
latter two drugs can promote uterine cancer, while raloxifene actually should
help prevent it, and is therefore a superior drug for women. It is not known how
effective it may be in increasing LH production.
While on high dose androgens it is impossible to maintain LH production in any
case, and clomiphene can do no good in that regard. As androgen levels return to
normal, however, a dose of 50 mg/day of clomiphene if estrogen levels are
reasonable, or 100 mg/day if estrogen levels are high, is usually effective in
restoring natural testosterone production.
Because the drug has a long half-life, when one takes 50 mg/day the amount in
the system is not only the 50 mg just taken, but also approximately another 250
mg from previous days. Thus, to immediately arrive at the therapeutic level, one
would take 300 mg (50 mg six times) on the first day, and then continue with 50
A small percentage of individuals suffer vision problems from use of clomiphene,
which is generally reversible upon discontinuance. These persons, of course,
should not use the drug after discovering the problem.
It also must be pointed out that these are prescription drugs, and should be
obtained and used only by precription with medical advice, though the selective
estrogen receptor modulators have excellent safety records.
After a cycle, it is reasonable to continue clomiphene use until at least four
weeks after the last injection of long acting ester, or at least two weeks after
the last use of an oral, or until natural testosterone production is clearly
back to normal, whichever comes last.
Other than acne and accelerated hair loss, the two most common problems of AAS
use are gynecomastia and difficulty in recovering natural testosterone
production. Antiestrogenic drugs can effectively address both problems and are
safe for most individuals. Ideally, if aromatizable drugs are used, the problem
is corrected at the source by limiting production of estrogen by using an
aromatase inhibitor. However, it is also effective to use a selective estrogen
receptor modulator such as Clomid. The latter drug is also of particular use in
helping to restore natural testosterone production after a cycle
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